Research progress in treatment of chronic myeloid leukemia patients with imatinib resistance

Abstract

Chronic myeloid leukemia (CML) is a malignant myeloproliferative neoplasm that occurs in pluripotent hematopoietic stem cells. Pathogenesis of CML is slow, and leukocytosis and splenomegaly are main clinical features of patients with CML. The introduction of tyrosine kinase inhibitor (TKI) imatinib mesylate (IM) has changed the natural progression of CML and significantly improved survival of CML patients. However, with the prolonged application of IM, IM resistance has become a major challenge in the treatment of CML. Many studies are currently working to elucidate the mechanisms of CML resistance and to research and develop new TKI. There is a urgent need to replace new drug targets and new therapeutic strategies for BCR/ABL1 fusion gene in response to IM-resistant CML patients. This article focuses on the development of CML-related TKI and non-TKI latest drugs for IM-resistant CML patients, and describes immunological approaches activating specific T cell responses against CML cells. Key words: Leukemia, myelogenous, chronic, BCR-ABL positive; Receptor protein-tyrosine kinases; Drug resistance, neoplasm; Immunotherapy; Therapeutic uses